M104 T3 L3 Flashcards
1
Q
Which arteriole in the kidney is narrower?
A
the efferent arteriole
2
Q
Why it is useful that the afferent arteriole in the kidney is narrower?
A
it causes a pressure to build up in the nephrons
3
Q
What is the difference between the afferent and efferent arterioles in the kidneys?
A
afferent - blood travels in and is filtered under-pressure
efferent - exit
4
Q
What is an effect of the afferent arteriole in the kidney being narrower?
A
blood traveling in through it is filtered under-pressure, so it can’t leave as easily
5
Q
What is the pressure that builds up due to the narrowing of the efferent arteriole?
A
10 mmHg
6
Q
What two features is filtration force in the nephrons determined by?
A
Blood pressure
Differing diameter of afferent and efferent arterioles
7
Q
What is the normal Glomerular Filtration Rate of all the glomerulae in the kidneys?
A
125 mL/min (180 L/day)
8
Q
What is the normal plasma volume?
A
2-3 L
9
Q
What is the Glomerular Filtration Rate used to indicate?
A
renal function when measured clinically
10
Q
What small molecules are filtered in ultrafiltration?
A
Glucose, electrolytes, metabolites (GEM)
Some drugs, amacs, Metabolic waste (SAM)
11
Q
What is the first stage of filtration?
A
Ultrafiltration
12
Q
What substances remain in the blood after ultrafiltration?
A
RBCs, lipids, proteins, most drugs, metabolites
13
Q
What barriers does filtrate have to pass through?
A
the glomerular capillary endothelium via small pores
the basement membrane of Bowman’s capsule
(includes contractile mesangial cells)
podocytes via filtration slits into capsular space
14
Q
What is the diameter of the pores in the endothelium of the glomerular capillary?
A
60um
15
Q
What is the effect of the contractile properties of mesangial cells?
A
they have been shown to be insignificant in changing the filtration pressure of the glomerulus
16
Q
What structures interdigitate with themselves?
A
pedicels - they join together but they have small gaps between them
17
Q
What structure results from the gaps between interdigitated pedicels?
A
filtration slits
18
Q
What is the role of filtration slits?
A
they allow molecules to come through the pedicels
19
Q
Why are podocytes susceptible to damage?
A
bc they are very specialized and very sensitive cells
20
Q
When might podocytes be damaged?
A
certain renal diseases, e.g. diabetes
21
Q
How can diabetes damage podocytes?
A
a high glucose level in circulation is filtered through podocytes during the filtration process
podocytes get poisoned by high glucose
this leaves gaps in the glomerular membrane, which allows proteins to leak through
22
Q
What happens to podocytes when exposed to high glucose levels?
A
they get poisoned and can die, break off and come out into the urine
23
Q
Where is the glomerular membrane located?
A
at the top of the nephrons
24
Q
What happens to diabetics as kidney disease gets worse?
A
more and more podocytes die off and aren’t replaced
25
What happens as a result of podocytes dying off?
Albuminuria from protein urea in the urine
26
How often are urine protein amounts measured in diabetic patients?
every six months
27
What is it an indication of if a diabetic patient's protein levels start to increase?
that some kidney disease is developing
28
How is the PGC calculated?
normal body BP + extra pressure from the narrow efferent arteriole
29
What does PGC measure?
the hydrostatic pressure of blood in the glomerular capillary
30
How does oncotic pressure work?
```
circulatory proteins (mostly albumin) in blood plasma exert oncotic pressure
this displaces water molecules, creating a relative h2o mlc deficit with water molecules moving back into the circulatory system within the lower venous pressure end of capillaries
```
31
Why is oncotic pressure higher in the glomerular capillary than in Bowman's capsule?
bc there is lots of albumin which gets left behind and doesn't get filtered
32
Why is the oncotic pressure of the Bowmans capsule almost zero?
bc there are hardly any proteins in the top of the nephron bc in healthy people the proteins don't leak through
33
What is the main glomerular pressure?
the pressure of the blood coming through when the glomerular capillaries push fluids through
34
What is the equation of filtration pressure?
(PGC + πBS) – (PBS + πGC)
35
What four factors contribute to filtration pressure?
PGC
πBS
PBS
πGC
36
What is the equation of filtration pressure when oncotic pressure is nearly equal to zero?
PGC – (PBS + πGC)
37
What is the hydrostatic pressure in a nephron?
45 mmHg
38
What is the osmotic pressure in a nephron?
25 mmHg
39
What is the hydrostatic pressure in a nephron?
10 mmHg
40
What is the net filtration pressure in a nephron?
10 mmHg
41
What is the net filtration pressure in a nephron calculated?
45 - 25 - 10 = 10 mmHg
42
How is filtration pressure calculated?
(PGC + πBS) – (PBS + πGC)
| the bp in the glomerular capillaries minus the two pressures pushing back the other way against it
43
What is normal bp?
120 / 80
44
What is the rate at which filtrate is produced in the kidneys?
125 mL/min (180 L/day)
45
What happens to the GFR and renal blood flow as circulatory bp changes?
they stay quite constant
46
What happens to the GFR and renal blood flow as systemic bp changes?
they stay quite constant via autoregulation
47
Over what range of systemic bps is GFR and renal blood flow under autoregulation?
broad range of 90-200 mmHg
48
In what circumstances will the NS in the kidneys be impaired?
if the NS (renal nerve) has been removed
isolated perfuse kidneys
in conditions where the renal nerve has been removed / damaged
49
What is the autoregulation of GFR and renal blood flow NOT controlled by and why?
the NS bc in kidneys where the NS is impaired / removed, autoregulation still occurs
neuronal or hormonal bc the autoregulation doesn't respond to any hormones circulating in the blood system
50
In what circumstances will the NS in the kidneys be impaired?
if the NS (renal nerve) has been removed
isolated perfuse kidneys
in conditions where the renal nerve has been removed / damaged
51
How is the autoregulation of GFR and renal blood flow established in the kidneys?
the kidney has a way of adjusting its blood system and the diameter of the renal artery according to the body's bp to ensure that it keeps getting the same blood flow, even if the body's bp is changing in a particular way
52
What are the two hypotheses that explain how the GFR and renal blood flow is autoregulated?
Myogenic
| Metabolic
53
What does the Myogenic hypotheses state?
that the autoregulation of GFR and renal blood flow is due to response of renal arterioles to stretch (Frank–Starling law of the heart)
54
What happens to the renal artery and efferent arterioles when bp decreases, according to the Myogenic hypotheses?
they automatically constrict to maintain a constant renal blood flow and GFR
55
What does the Metabolic hypotheses state?
that afferent & efferent arteriolar contraction / dilation is modulated by renal metabolites
56
What is the constant renal blood flow?
1200mL/min
57
What is the GFR?
~125 mL/min
58
What are examples of renal metabolites that involved in the Metabolic hypotheses?
adenosine, nitric oxide
59
What is the likely way in which the GFR and renal blood flow is autoregulated?
Most likely to be a combination of both hypotheses (metabolic & myogenic)
60
What happens to the autoregulation of the GFR and renal blood flow below the range of 90-200 mmHg?
the system breaks down and renal function declines
61
What happens to the autoregulation of the GFR and renal blood flow above the range of 90-200 mmHg?
renal function goes out of control and can damage internal renal structures, causing blood loss and damage within the kidney structures
62
What substances is natriuresis is promoted by?
ventricular and atrial natriuretic peptides
| calcitonin
63
What is an example of a substance natriuresis is inhibited by?
aldosterone
64
Where is atrial natriuretic peptide secreted from?
the atria
65
What is the main function of atrial natriuretic peptide?
reduces ECF volume by increasing renal sodium excretion
66
How do kinins affect the circulatory system?
they affect bp pressure (especially low bp)
they increase blood flow throughout the body
they make it easier for fluids to pass through small blood vessels
67
What happens to inflow blood (via the afferent arteriole) when the GFR is low?
specific vasodilators are released, the afferent artery dilates
Angiotensin II is released, the efferent artery constricts
68
Where is atrial natriuretic peptide secreted from?
the atria
69
What is the main function of atrial natriuretic peptide?
reduces ECF volume by increasing renal sodium excretion
70
How do kinins affect the circulatory system?
they affect bp (especially low bp)
they increase blood flow throughout the body
they make it easier for fluids to pass through small blood vessels
71
Afferent arteriole
GFR
| e.g. due to BP
72
What vasodilators are released when the GFR is low? (PAKD.NO)
Prostaglandins, ANP, kinins, dopamine, NO
73
What happens to outflow blood (via the efferent arteriole) when the GFR is high?
specific vasoconstrictors are released, the afferent artery constricts
adenosine & NO are released, the efferent artery dilates
74
What vasoconstrictors are released when the GFR is high?
noradrenaline , endothelin, adenosine (via A1 receptors), ADH
75
What receptors are responsible for the release of adenosine as a vasoconstrictor?
A1 receptors
76
What nerves are responsible for the release of noradrenaline?
the sympathetic nerves
77
What receptors are responsible for the release of adenosine as a vasodilator?
A2A & A2B receptors
78
How does a drop in the GFR alter the systemic bp and how is the GFR affected after?
AAR, less Na+ enters the proximal tubule
the macula densa senses a change in tubular Na+ levels
stimulates juxtaglomerular cells to release renin into the blood, which makes angiotensinogen, is converted to angiotensin I
goes to the lungs via circulation where ACE is present
gets converted to Ang II
acts as a vasoconstrictor, pushes up the BP, causes filtration pressure to increase
GFR returns to normal
79
What causes a drop in GFR?
a drop in filtration pressure (e.g. due to declining BP)
80
What are juxtaglomerular cells otherwise known as?
JG cells
| granular cells
81
What is the function of juxtaglomerular cells?
to synthesize, store, and secrete renin. They are (and some in the efferent arterioles) that deliver blood to the glomerulus.
82
Where are juxtaglomerular cells located?
in the kidney, mainly in the walls of the afferent arterioles
83
What is the effect of a drop in the GFR on the systemic bp?
it increases due to Ang II and vasoconstriction
84
What process is responsible for enacting negative feedback when there is a drop in the GFR?
the Renin-Angiotensin System
85
What are features of angiotensin II?
is an extremely active, and a very small molecule
| is very powerful bc it has lots of effects that increase the bp
86
How does angiotensin II act as a vasoconstrictor?
it acts on the symp NS so that the symp nerves release more adr
87
How does Ang II increase reabsorption of Na+ and water in the kidneys?
it increases Na+ reabsorption, so more salt re-enters the circulation
this causes water to re-enter the circulation from glomerular filtrate that builds up the circulating volume
this pushes bp up
makes the adrenal gland release aldosterone which also causes Na+ reabsorbtion, etc, further pushes bp up
AAR, the pituitary gland releases AHD, which further encourages reabsorption in the kidneys
Na+ reabsorption < water reabsorption < bp up < aldosterone (adrenal gland) < more reabsorption < ADH (pituitary gland) < more reabsorption
88
What is the effect of angiotensin II on thirst?
it works in the brain to increase thirst
results in drinking more fluids, which will enter your circulation and have a long term effect of bringing bp back up towards normal
89
What is the effect of hypertension on the RAAS system?
can cause it to become disregulated, overstimulated
90
Why does hypertension overstimulate the RAAS system?
bc the sympathetic NS is triggered all over the body and within the kidney, which causes more renin to be released and it kicks off the whole system of generating too much angiotensin
91
What does ARB stand for?
angiotensin 2 receptor blockers
92
What are examples of ACE inhibitor drugs that can be used to stop hypertension overstimulating the RAAS system?
captopril and enalapril (-pril drugs)
93
What is the role of ACE inhibitor drugs?
they inhibit angiotensin converting enzymes in the lungs
94
What are examples of ARB drugs that can be used to stop hypertension overstimulating the RAAS system?
sartan drugs like losartan
95
What is the effect of sartan drugs?
they act as antagonists on the AT1 receptor - the receptors that Angiotensin 2 works on
96
What is the receptor of Ang II?
AT1 receptor
97
What type of drugs are most drug names that end in --pril?
ACE inhibitors
98
What groups of drugs are used to stop hypertension from overstimulating the RAAS system?
```
ACE inhibitors (-pril)
kiren drugs
ARB drugs (sartans)
```
99
How do kiren drugs work?
they are renin inhibitors
100
What is an example of a kiren drugs that can be used to stop hypertension overstimulating the RAAS system?
aliskiren
101
What is behind the driving force of reabsorption from the proximal tubule?
Na+K+ATPase
102
What substances is there almost complete reabsorption of in the PT?
glucose, amacs, small amount of filtered Proteins (GAP)
103
What substances is there almost complete reabsorption of in the PT?
glucose, amacs, small amount of filtered Proteins (GAP)
104
What is the role of Na+-K+-ATPase?
to pump out Na+ from cells into the blood against chemical and electrical gradients
105
What does Na+-K+-ATPase require to work?
E - ATP
106
How does Na+-K+-ATPase work?
Na+ leaves the cell with Cl- (salt)
| K+ enters with ATP
107
What is the ratio of transport of Na:K in and out of the cell via Na+-K+-ATPase?
3 Na+ leaves, 2 K+ enters
108
What is the intracellular Na+ concentration in PT cells?
less than 30 mM (very low)
109
Why is the intracellular Na+ concentration in PT cells really low?
due to the action of the Na+K+ATPase
110
What is the relationship between Na+-K+-ATPase and water movement?
Na+ leaves the cell with Cl- (salt) to enter the peritubular capillaries
water likes to follow the salt bc of the high conc of salt outside of the cells, so it gets dragged through aquaporins and makes it more dilute
111
What substances travel through Na+/glucose co-transporters and where to?
glucose travels with sodium into the cell
112
What are features of the Na+/glucose co-transporters?
it works all the time and is very powerful
113
What is the role of the Na+/glucose co-transporters?
to keep the inside of the proximal tubular cell at a low Na+ conc - at less than 30 mM instead of 150 mM around the glomerular filtrate site
114
What happens when the inside of the proximal tubular cell has a lower Na+ conc?
all the filtered sodium coming through from the glomerulus wants to enter the cells bc they have a low concentration
115
How does Na in the inside of the proximal tubular cell leave?
it is pumped out into the peritubular capillary from the base / the lateral side of the pump
116
How does Na enter the inside of the proximal tubular cell when it has a lower Na+ conc than the glomerular filtrate?
via a detraction conc grad
| via an electrochemical gradient
117
Why are proximal tubular cells so negative?
bc it is packed full of -vely charged transport proteins that also make up the mitochondria
118
What is the overall charge in proximal tubular cells?
-70 mV
119
What is the overall charge in glomerular filtrate and why?
the overall charge is +ve bc Na+ is a positive ion and there's lots of it in the glomerular filtrate
120
How does Na enter the proximal tubular cells against its conc grad from the glomerular filtrate via an electrochemical gradient?
the prox. tubular cells are -70mV but glomerular filtrate is positive - opposites attract
121
Where are aquaporin channels located?
on the apical and basolateral surfaces of the kidney cells
122
What does the movement of solutes (Na+, HCO3-
| and Cl-) from glomerular filtrate into the proximal tubular cells achieve?
it reduces osmolality of tubular fluid and increases osmolality of interstitial fluid
123
By what routes does the net flow of water from the tubule lumen to lateral spaces occur?
transcellular and paracellular routes
124
What are features of the transcellular routes by which water flows from the tubule lumen to lateral spaces?
aquaporin channels
125
How is water reabsorbed along the nephron?
osmosis / follows Na+
126
How many different types of aquaporins have been identified?
thirteen
127
How many different types of aquaporins are present in the kidney?
six
128
What are the four major renal types of aquaporins?
AQP1, AQP2, AQP3 & AQP4
129
Where are Aquaporin-1s located?
they have an abundant distribution in the proximal tubule, and other parts of the tubule where water is reabsorbed, e.g. descending limb of LOH
130
Where are Aquaporin-2s located?
in the collecting duct on the apical surface
131
What substance is AQP-2 channel expression controlled by?
antidiuretic hormone
| according to how dehydrated the person is
132
Where are Aquaporin-3s & 4s located?
on the basolateral surface of tubular cells involved in water reabsorption
133
How is glucose reabsorbed into the peritubular capillary?
via a glucose transporter
134
Why is there a low concentration of glucose in the peritubular capillary?
bc it has been filtered up the glomerulus
135
Once in the peritubular capillary, how does glucose re-enter the blood?
via a Na co-transporter
136
What percentage of available glucose is reabsorbed via the SGLT2 cotransporter in S1?
90% bc the body needs that glucose
137
What are the two parts of the proximal tubule?
the PCT & the proximal straight tubule PST
138
What transporters are responsible for the movement of glucose in Segment 1?
SGLT2, cotransports Na+ with glucose into the cell
139
What is S1 otherwise known as?
segment 1
| the proximal convoluted tubule (PCT)
140
What is a feature of the SGLT2 cotransporter?
a very powerful pump
141
What makes the SGLT2 cotransporter a very powerful pump?
it has a low affinity and a high capacity
| so it only needs small amounts of Na+ to transport a large amount of glucose
142
What percentage of available glucose is left behind from the SGLT2 cotransporter in S1?
10%
143
What happens to the left over glucose (10%) that is not reabsorbed by the SGLT2 cotransporter in S1?
it's caught lower down in Segment 3, which has SGLT1 transporters
144
What is a feature of the SGLT2 cotransporter?
high affinity, low capacity
145
Where are the SGLT2 cotransporters located?
in Segment 1 / the PCT
146
Where are the SGLT1 cotransporters located?
in Segment 3 / the PST
147
What percentage of available glucose is reabsorbed in total?
100% bc the body needs that glucose
148
What substances are transported by the SGLT2 cotransporter?
Na+ is transported with one glucose
149
How much glucose is excreted in urine in healthy people?
very little
150
What happens if a diabetic patient has excessive glucose in their circulation?
when undergoing filtering in the proximal tubules, the SGLT transporters will get filled up to their maximum limit for transportation and so will be working at full capacity - their transport maximum
however, often, it is not enough to reabsorb all the glucose that's being filtered in higher amounts (due to diabetes)
151
What is the normal plasma glucose concentration range in healthy patients?
5-10mM (5 or 6mM)
152
What percentage of plasma glucose is reabsorbed up to about 10 mM?
100% - almost all
153
How high will the plasma glucose concentration increase to after a sugary meal / drink?
up to about 10 mM
154
What is the approximate plasma glucose concentration range in diabetic patients after a sugary meal?
20-30 mM
155
What happens when plasma glucose concentration levels reach 20-30 mM after a sugary meal?
glucose transportation reaches a limit and discontinues, so glucose starts to appear in urine
156
How do blood urine tests work?
a dipstick is used to look at glucose urine levels
157
How is diabetes diagnosed?
blood urine tests will pick up any glucose in the patient's urine
158
What does a blood urine test that does not detect any diabetes in the urine indicate?
that the patient is healthy
159
What is the long-term effect of diabetics continually excreting glucose?
it will eventually bring the blood glucose levels down, bc if glucose is continually excreted, it will eventually leave the body, having a beneficial effect - hypoglycaemic effect
160
What are examples of drugs used to treat diabetes?
biguanides (metformin only)
| insulin injections
161
How do the biguanide drugs work?
by reducing the production of glucose that occurs during digestion
162
What is the only biguanide currently available in most countries for treating diabetes?
Metformin
163
Is Metformin a short or long term treatment of diabetes?
it needs to be taken long-term (years)
164
Does metformin have any side-effects?
mild and serious side effects, which are the same in men and women
165
What are examples of metformin side-effects?
```
diarrhoea, flatulence
stomach pain, nausea, vomiting
bloating, heartburn
gas
diarrhoea
constipation
weight loss
```
166
Where does glucose transport / reabsorption occur?
in the proximal tubules
167
What is an example of a drug that was previously used to treat diabetes II?
phlorizin
168
How does phlorizin work?
they accessed / got into the glomerular filtrate and were secreted into the proximal tubule where they would block thee Na/glucose transporters
169
How does phlorizin work?
they accessed / got into the glomerular filtrate and were secreted into the proximal tubule where they would block thee Na/glucose transporters in the proximal tubular cells so that this glucose couldn't be absorbed and would come out in the urine
170
What class of drugs have been developed to treat diabetes II?
the flozin drugs
171
What are the three main flozins used in the West to treat diabetes II?
Dapagliflozin
Canagliflozin
Empagliflozin (BI-10773)
172
What type of drugs are the flozins?
SGLT2 inhibitors
173
What is the main flozin used in Japan to treat diabetes II?
Empagliflozin
174
How do flozins work?
they block the SGLT2 transporters in the kidneys to stop the glucose being reabsorbed so that glucose comes out in the urine and not so much enters the blood (which is the goal)
175
Which developmental diabetes drug was withdrawn/cancelled?
sotagliflozin
176
Why was sotagliflozin withdrawn / cancelled?
bc it caused liver toxicity in clinical trials
177
Why is having sugary urine potentially dangerous?
bc it makes patients more susceptible to UTIs bc bugs
| like sugary solutions
178
Why are SGLT2 inhibitors used even though having sugary urine is potentially dangerous?
bc the benefits of these drugs seem to outweigh the risk of UTIs
bc any UTIs can be treated with antibiotics and good personal hygiene
bc it's not normally a problem
179
Why are SGLT2 inhibitors potentially dangerous?
bc their aim is to cause sugary urine which can lead to UTIs sometimes
bc it can be misused by healthy people illegally was a way to lose weight
180
What are alternative uses of SGLT2 inhibitors?
they can be used to lose weight - can be abused, bc if glucose is removed from the system in healthy people, it won't be converted to fat etc and will result in weight loss
181
Why are SGLT2 inhibitors dangerous to use for weight loss?
it leads to hypoglycaemia if used in healthy people or if misused - this can cause real issues of brain glucose loss that can lead to coma
182
Why are SGLT2 inhibitors potentially not very effective independently?
bc it elicits an adaptive increase in E intake - e.g. increased appetite
183
Why are SGLT2 inhibitors a very popular treatment for diabetes II internationally?
bc they have actually been shown to help diabetic patients avoid diabetic complications in clinical trials, bc they seem to make the patients healthier
184
What are the effects of SGLT2 inhibitors on diabetes II patients in clinical trials?
they don't get as much kidney problems
they don't get as much eye retinopathy
their CVS profiles are much better
185
What percentage of urea is reabsorbed in the proximal tubule?
about 40 - 50%
186
How are amacs transported in and around the proximal tubule?
via their independent transport system that involves endocytosis - proteins leak through from the glomerulus, so small amounts of proteins can be reabsorbed
187
How does endocytosis allow for the transportation of amacs?
the amacs have contact with the proximal tubular cell surface and enter it
then, as they travel through the proximal tube, they are broken down into amacs, which then are returned to the blood
188
What kinds of substances can't be filtered at the glomerulus?
some endogenous substances and drugs
189
Why can't some substances be filtered at the glomerulus?
bc of their size or protein binding
190
What two alternative specialised pumps are present in the PT?
one for organic acids
| one for organic bases
191
What are examples of substances that are transported by the organic acid pump in the PT?
uric acid, diuretics, antibiotics (penicillin)
192
What are examples of substances that are transported by the organic base pump in the PT?
creatinine, procainamide
193
In what areas of the body is OAT1 present? (PEKS.BPTC)
placenta, eyes, kidneys, smooth muscles
| brain, proximal tubular cells
194
What do the OAT1s control the excretion of?
common drugs, toxins, and endogenous metabolites into the urine
195
What is the role of URAT1?
a type of OAT located in renal PTCs, where it mediates the re-absorption of uric acid from the PT
196
What is the relationship between Na+ and a-KG?
when there is a low Na+ conc, it drags in alpha-ketaglutarate, which then is excreted by OAT pumps, which then drags in organic acid anions
197
What is the use of Para-aminohippurate?
a tool to measure tubular secretion
198
How is Para-aminohippurate processed before use?
it is IV infused
199
Is Para-aminohippurate produced by the body naturally?
no - it's an endogenous compound
200
How is it that PAH can be used as a marker of tubular secretion?
bc it's not filtered, it's only secreted into the PT and is transported
201
What is the pathway of Para-aminohippurate after administration?
it is transported into PT cells from blood with a-Kg / other di/tri carboxylates
is it then transported out of PT cells in exchange for another anion present in the PT lumen
202
How is it a result on PAH used after administration?
after administration, the amount that comes out in the urine is measured
203
What is the main setting where PAH is used?
in a clinical setting
204
In what circumstances might PAH be used?
when we want to measure how much of a drug is being transported out at the same time
a ratio is made and compared between the ratio for the excretion of the drug to the excretion / secretion of PAH
205
What are examples of endogenous organic acids that are secreted into urine by the PT? (COPP.HHUBs)
```
cAMP
Oxalate
Procainamide
Prostaglandins
Hippurates (not PAH - synthetic)
Hydrochlorothiazide
Urate (Uric acid)
Bile salts
```
206
What are examples of organic acid drugs that are secreted into urine by the PT? (CABS. FPPP)
```
Chlorothiazide
Acetozolamide
Bumetanide
Salicylate (Aspirin)
Furosemide
Penicillin
Probencid
PAH
```
207
What are examples of endogenous organic bases that are secreted into urine by the PT? (ACD,GHNT)
```
Adrenaline (Epinephrine)
Creatinine, Choline
Dopamine
Guanidine
Histamine
Noradrenaline (Norepinephrine)
Thiamine
```
208
What are examples of organic base drugs that are secreted into urine by the PT? (MAP.QICA)
```
Morphine
Atropine
Procainamide
Quinine
Isoproterenol
Cimetidine
Amiloride
```
209
What is the overexpression of AT1 receptors associated with?
risk factors such as hypertension, hypercholesterolae- mia, and diabetes
210
What happens when there's a drop in the GFR?
RAS is activated and is responsible for enacting negative feedback to increase the GFR back to normal levels
211
What substance does angiotensin stimulate the release of?
aldosterone
212
From where is aldosterone released?
the adrenal cortex
213
Why does angiotensin stimulate aldosterone release?
to promote sodium retention by the kidneys
